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IPT: Renal > Block 2 > Flashcards

Block 2 Flashcards

1
Q

Per KDIGO, what is acute kidney injury?

A
  1. Increase SCr ≥0.3mg/dL within 48hrs
  2. Increase SCr ≥1.5 times baseline within 7 days
  3. Urine volume <0.5mL/kg/hr for 6 hrs
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2
Q

What is an nonoliguric urine output?

A

> 500mL / 24hrs

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3
Q

What is an oliguric urine output?

A

50 to 500mL / 24hrs

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4
Q

What a an anuric urine output?

A

<50mL / 24hrs

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5
Q

What are some risk factors for AKI?

A

Diabetes, HTN, Age >65yrs, AA, UT obstruction, volume depletion

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6
Q

What does RIFLE stand for?

A 
Risk
Injury
Failure
Loss
ESRD
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7
Q

Describe R in RIFLE

A

UOP:
<0.5mL/kg/hr for 6 hrs

SCr:
1.5-2x increase from base OR Increase by ≥0.3mg/dL

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8
Q

Describe I in RIFLE

A

UOP:
<0.5mL/kg/hr for 12 hrs

SCr:
2-3x increase from base

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9
Q

Describe F in RIFLE

A

UOP:
<0.3mL/kg/hr for 24 hrs OR anuria for 12 hrs

SCr:
>3x increase from base OR if SCr is >4 w/ acute rise ≥0.5 OR if pt is on RRT

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10
Q

Describe L in RIFLE

A

Persistent renal failure for >4 weeks

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11
Q

Describe E in RIFLE

A

Persistent renal failure for >3 months

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12
Q

Where is the highest % of incidence with regards to AKI?

A

ICU-acquired

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13
Q

Where is the lowest survival rate with regards to AKI?

A

ICU-acquired

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14
Q

Where is the highest survival rate with regards to AKI?

A

Community-acquired

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15
Q

Prerenal
Intrinsic
Postrenal

Actual or functional intravascular volume depletion

A

Prerenal

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16
Q

Prerenal
Intrinsic
Postrenal

Acute interstitial nephritis or tubular necrosis

A

Intrinsic

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17
Q

Prerenal
Intrinsic
Postrenal

Obstruction preventing outflow

A

Postrenal

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18
Q

Prerenal
Intrinsic
Postrenal

Most common AKI

A

Prerenal

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19
Q

Prerenal
Intrinsic
Postrenal

Least common AKI

A

Postrenal

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20
Q

Which drug classes can cause prerenal AKI?

A

NSAIDS + ACE inhibitors

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21
Q

Which drug classes can cause intrinsic AKI?

A

Nephrotoxins such as antibiotics (aminoglycosides) or contrast

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22
Q

Prerenal
Intrinsic
Postrenal

Cancer could cause which one?

A

Postrenal

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23
Q

Prerenal
Intrinsic
Postrenal

Which one has a BUN/SCr ratio >20:1

A

Prerenal

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24
Q

Prerenal
Intrinsic
Postrenal

Which one has a BUN/SCr ratio <20:1

A

Intrinsic + Postrenal

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25
Q

Prerenal
Intrinsic
Postrenal

Which one has <20 mmol/L of sodium in urine?

A

Prerenal

**<1% of FENa

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26
Q

Prerenal
Intrinsic
Postrenal

Which one has >40 mmol/L of sodium in urine?

A

Intrinsic + Postrenal

**>2% of FENa

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27
Q

How do you calculate FENa?

A

100 x (Na of Urine) x (Cr of Plasma) / (Na of Plasma) x (Cr of Urine)

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28
Q

Prerenal
Intrinsic
Postrenal

Which one’s function usually returns?

A

Prerenal + Postrenal

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29
Q

Prerenal
Intrinsic
Postrenal

Which one typically has a less favorable prognosis?

A

Intrinsic

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30
Q

What is the goal MAP for AKI?

A

> 65 mmHg

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31
Q

When should you use loop diuretics to treat AKI?

A

In hypervolemic pt w/ oliguria or non-oliguria

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32
Q

What are the 4 main things you could use to treat contrast-induced nephropathy?

A
  1. NS
  2. Sodium Bicarb
  3. N-acetylcysteine
  4. Rosuvastatin
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33
Q

How would you order a bicarb fluid for contrast-induced nephropathy?

A

Order 154mEq Bicarb in D5W @ 3mL/kg/hr x 1 hr prior to contrast, then to 1mL/kg/hr during contrast exposure and for 6 hours after

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34
Q

How would you order N-acetylcysteine for contrast-induced nephropathy?

A

600mg PO BID x 4 doses (3 before, 1 after) for CKD pt

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35
Q

How would you order rosuvastatin for contrast-induced nephropathy?

A

10mg PO QPM x 5 days (2 before, 3 after) for CKD pt

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36
Q

Which systems can produce ROS?

A

NADPH + Mitochondrial

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37
Q

Which complexes in the mitochondria produce ROS? Where specifically?

A

1 (intermembrane space) and 3 (matrix)

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38
Q

What is the mechanism of injury for aminoglycosides?

A
  • Accumulates RX within proximal tubular epithelial cells
  • Toxicity is related to positive charge of drug as they bind to negatively charged phospholipids – this binding induces transportation of lysosomes
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39
Q

Which side of the glomerulus does cyclosporine affect?

A

Afferent vasoconstriction

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40
Q

Which side of the glomerulus does tacrolimus affect?

A

Afferent vasoconstriction

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41
Q

Which drug is B cell mediated?

A

Allopurinol

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42
Q

What is the pH range of urine?

A

4.5 to 7.8

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43
Q

Elevated pH of urine may indicate what?

A

Urea-splitting bacteria

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44
Q

Elevated specific gravity of urine may indicate what?

A

Dehydration

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45
Q

What is the normal range of SCr?

A

0.6 to 1.2mg/dL

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46
Q

As you age, what happens do your daily creatinine production?

A

It decreases

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47
Q

What is the normal range of BUN?

A

6 to 20 mg/dL

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48
Q

What are the stages for CKD?

A 
G1 = >90mL/min/1.73m2
G2 = 60-89
G3a = 45-59
G3b = 30-44
G4 = 15-29
G5 = <15
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49
Q

When should you use the Jeliffe equation?

A

If pt height or weight are unknown, may be useful in unstable renal function

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50
Q

When should you use the Schwartz equation?

A

Calculating for pediatric or adolescent patients

51
Q

What is the name of vitamin D that the liver produces?

A

25-Hydroxyvitamin D3

52
Q

What is the name of vitamin D that the kidney produces?

A

1,25-Dihydroxyvitamin D3

53
Q

What is needed to facilitates calcium absorption from the gut?

A

Vitamin D

54
Q

Parathyroid (stimulate) + Calcium, what is the concentration in serum and urine?

A

Increase serum concentration and decrease urine concentration

55
Q

How does cinacalcet work?

A

Reduces parathyroid and serum calcium

56
Q

How is epoetin and darbepoetin alfa made?

A

Recombinant DNA technology

57
Q

Epoetin vs Darbepoetin

Which one is identical to EPO?

A

Epoetin alfa

58
Q

Epoetin vs Darbepoetin

Which one is the modified form of EPO?

A

Darbepoetin alfa

59
Q

What is the most common inpatient type of drug-induced kidney injury?

A

Acute tubular necrosis

60
Q

What is the incidence rate of aminoglycoside-related DIKI?

A

2-58%

61
Q

What is the incidence rate of cisplatin/carboplatin-related DIKI?

A

6-13%

62
Q

What is the incidence rate of amphotericin B-related DIKI?

A

80% w/ prolonged use

63
Q

How does aminoglycoside cause renal damage?

A

Cation binds to tubules

64
Q

How does amphotericin B cause renal damage?

A

Arterial vasoconstriction + direct

65
Q

How do you prevent renal damage when using aminoglycosides?

A

Use one big dose rather than prolonged therapy

66
Q

How do you prevent renal damage when using amphotericin B?

A

Slow down the infusion

67
Q

What is the incidence rate of contrast-related DIKI?

A

2-50%

68
Q

What RX should you avoid when using contrast?

A

Metformin

69
Q

What are some prevention methods for acute tubular necrosis?

A
  1. Hydrate
  2. Acetylcysteine
  3. Statin
  4. Ascorbic acid
70
Q

What RX can cause allergic interstitial nephritis?

A

Beta lactams + NSAIDs

71
Q

How do you treat allergic interstitial nephritis?

A

Corticosteroids and d/c offending agent

72
Q

What RX can cause chronic interstitial nephritis?

A

Lithium + Cyclosporine

73
Q

What RX can cause renal vasculitis?

A
  1. Hydralazine
  2. Allopurinol
  3. Propylthiouracil
  4. Warfarin
74
Q

How do you treat renal vasculitis?

A
  1. Corticosteroids
  2. Antiplatelets
  3. Plasmapheresis
  4. IVIG
75
Q

What RX can cause obstructive nephropathy?

A
  1. Sulfonamides
  2. Acyclovir + Indinavir
  3. Methotrexate
  4. Ascorbic acid
76
Q

How do you treat obstructive nephropathy?

A
  1. Hydrate
  2. d/c offending agent
  3. Urine alkalization
77
Q

What does fibroblast growth factor 23 do?

A

Decreases serum phosphorus

78
Q

What is the main goal for CKD?

A

To delay or halt progression of CKD

79
Q

What are some things to watch out for when using ESAs?

A

Higher % of HTN, Hb, MI

Watch Hb and make sure it doesnt go over 13!!!! Increased CV events

80
Q

ESA treatment and Hb monitoring

A

Acceptable rate of increase should be 1 to 2g/dL per month, increases dose if it doesnt rise by 1g/dL in weeks

Should not exceed 1g/dL in 2 weeks

81
Q

CKD Stage 3a/3b, what is the corrected calcium level?

A

Within normal range

82
Q

CKD Stage 4, what is the corrected calcium level?

A

Within normal range

83
Q

CKD Stage 5, what is the corrected calcium level?

A

8.4 to 9.5

84
Q

CKD Stage 3a/3b, what is the phosphorus level?

A

2.7 to 4.6

85
Q

CKD Stage 4, what is the phosphorus level?

A

2.7 to 4.6

86
Q

CKD Stage 5, what is the phosphorus level?

A

3.5 to 5.5

87
Q

CKD Stage 3a/3b, what is the Ca x P level?

A

<55 for all stages

88
Q

CKD Stage 3a/3b, what is the intact PTH level?

A

35 to 70

89
Q

CKD Stage 4, what is the intact PTH level?

A

70 to 110

90
Q

CKD Stage 5, what is the intact PTH level?

A

150 to 300

91
Q

When should you d/c or reduce dose of Aranesp?

A

Reduce dose by at least 25% if increased rate of Hb

92
Q

When should you increase dose of Aranesp?

A

If Hb is not rising by 1g/dL in 4 weeks and no causes of resistance

93
Q

What is the level of 25(OH) D found in CKD level 3,4, and 5?

A

> 30

94
Q

If someone has iron deficiency while using an ESA agent, what should you correct first?

A

Iron

95
Q

When should you start using Sevelamer (Renvela) for pt with CKD-MBD?

A

Ca x P >55

Primary therapy in CKD Stage G5

96
Q

What are some issues with using aluminum hydroxide for pt with CKD-MBD?

A

Risk of aluminum toxicity

Do not use with citrate-containing products

97
Q

When should a pt use aluminum hydroxide if they have CKD-MBD?

A

For short term (<4wks) with hyperphosphatemia not responding to other binders

98
Q

What are the non-calcium containing RX for CKD-MBD?

A

Ferric Citrate, Sevelamer (Renvela), Lanthanum, and Aluminum hydroxide

99
Q

What are some comments to know about ferric citrate?

A

Do not take more than 12 tabs/day

Iron-containing; may reduce ESA and iron dosing

Expensive

100
Q

What are some things to watch out for when using Sevelamer for CKD-MBD?

A

Removes bicarb, caution in metabolic acidotic pts

101
Q

When taking other RX with phosphate-binding agents for CKD-MBD, how should you administer the other medications?

A

1 hour before or 3 hours after

102
Q

What are some key counseling points with phosphate-binding agent?

A
  1. Take w/ meals or immediately prior to them

2. Avoid in pt w/ high CaxP (risk of calcification) or low PTH

103
Q

Brand of Ferric Citrate

A

Auryxia

104
Q

Generic of Auryxia

A

Ferric Citrate

105
Q

Brand of Lanthanum

A

Fosrenol

106
Q

Generic of Fosrenol

A

Lanthanum

107
Q

Brand of Aluminum hydroxide

A

AlternaGel

108
Q

Generic of AlternaGel

A

Aluminum hydroxide

109
Q

Brand of Sevelamer

A

Renvela

110
Q

Generic of Renvela

A

Sevelamer

111
Q

Brand of calcium acetate

A

PhosLo

112
Q

Generic of PhosLo

A

calcium acetate

113
Q

Which vitamin D analog has the highest chance of hypercalcemia?

A

Calcitriol

114
Q

Prior to starting vitamin D analogs, when should you consider withholding it?

A

If Ca x P >55

115
Q

MOA of Cinacalcet?

A

Increase sensitivity of serum Ca located on chief cells of parathyroid gland to reduce PTH secretion

116
Q

If a pt has a high level of Ca x P, could you give them Cinacalcet?

A

Yes

117
Q

When should you start monitoring pt once initiated w/ Cinacalcet?

A

ONLY FOR DIALYSIS PATIENTS

Within 1 week after initiation or dose change

PTH = within 1 to 4 weeks after initiation or dose adjustment

118
Q

What are some RX interactions w/ Cinacalcet?

A

CYP3A4 inhibitors + Rx that utilize CYP2D6

119
Q

MOA of Vitamin D analogs?

A

Promote calcium reabsorption + suppress PTH secretion

120
Q

MOA of Phosphate-binding agents?

A

Binds to dietary phosphorus in GI tract to form insoluble phosphate that is then excreted

121
Q

Cystatin C has been proven most useful in which condition?

A

Contrast-induced renal disease + cardiac disease

122
Q

What range of SCr would not be a good indicator of a patient’s true renal function?

A

<1

123
Q

When is the Salazar-Corcoran equation used?

A

For obese patients

124
Q

If a pt is not responding to an ESA agent, what could be the cause?

A
  1. Low iron
  2. Hyperparathyroidism
  3. Infection

IPT: Renal (3 decks)

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